Atrial fibrillation ventricular rate control

TABLE 6-5. Drugs for Ventricular Rate Control in Atrial Fibrillation... 

FIGURE 6-5. Decision algorithm for ventricular rate control using intravenous drug therapy for patients presenting with the first detected episode or an episode of persistent atrial fibrillation that is hemody-namically stable. 

FIGURE 6-6. Decision algorithm for long-term ventricular rate control with oral drug therapy for patients with paroxysmal or permanent atrial fibrillation, bpm, beats per minute CCB, calcium channel blocker (diltiazem or verapamil) HF, heart failure LV, left ventricular function LVEF, left ventricular ejection fraction. (Algorithm adapted with permission from Tisdale JE, Moser LR. Tachyarrhythmias. In Mueller BA, Bertch KE, Dunsworth TS, et al. (eds.) Pharmacotherapy Self-Assessment Program, 4th ed. Kansas City American College of Clinical Pharmacy 2001 ... 

Atrial fibrillation Peak digoxin body stores larger than the 8 to 12 mcg/kg required for most patients with heart failure and normal sinus rhythm have been used for control of ventricular rate in patients with atrial fibrillation. Titrate doses of digoxin used for the treatment of chronic atrial fibrillation to the minimum dose that achieves the desired ventricular rate control without causing undesirable side effects. Data are not available to establish the appropriate resting or exercise target rates that should be achieved. 

Treatment of atrial fibrillation is initiated to relieve patient symptoms and prevent the complications of thromboembolism and tachycardia-induced heart failure, the result of prolonged uncontrolled heart rates. The initial treatment objective is control of the ventricular response. This is usually achieved by use of a calcium channel-blocking drug alone or in combination with a 13-adrenergic blocker. Digoxin may be of value in the presence of heart failure. A second objective is a restoration and maintenance of normal sinus rhythm. Several studies show that rate control (maintenance of ventricular rate in the range of 60-80 bpm) has a better benefit-to-risk outcome than rhythm control (conversion to normal sinus rhythm) in the long-term health of patients with atrial fibrillation. If rhythm control is deemed desirable, sinus rhythm is usually restored by DC cardioversion in the USA in... 

Khan IA, Nair CK, Singh N, et al. Acute ventricular rate control in atrial fibrillation and atrial flutter. IntJ Cardiol. 2004 97 7-13. 

An example of this initial dosage scheme is provided in the following case. Mr. PO is a 72-year-old, 83-kg, 5-ft, 11-in man admitted to the hospital for the treatment of community-acquired pneumonia. While in the hospital, Mr. PO develops atrial fibrillation, and the decision is made to treat him with digoxin to provide ventricular rate control. His serum creatinine concentration is 2.5 mg/dL and stable. Calculate an intravenous loading dose and oral maintenance dose that will achieve a Cjj of 1.5 ng/mL. The Cockcroft-Gault equation can be... 

Patients with diastolic heart failure are typically dependent upon preload to maintain adequate cardiac output. While patients with symptomatic volume overload will benefit from careful modulation of intravascular volume, volume reduction should be accomplished gradually and treatment goals reassessed frequently. In addition to cautious volume management, it is important to maintain synchronous atrial contraction in such patients, which maintains adequate left ventricular filling during the latter phase of diastole. Cardiac function is often severely impaired if patients with diastolic heart failure develop atrial fibrillation, particularly in the context of sub-optimal ventricular rate control. Meticulous control of the ventricular rate with drugs that slow AV conduction is mandatory (see Chapter 34) and restoration of sinus rhythm should be considered. It is also important to evaluate and treat conditions that are associated with dynamic abnormalities of diastolic function, such as myocardial ischemia and poorly controlled systemic hypertension. 

In patients with HF and supraventricular tachyarrhythmias such as atrial fibrillation, digoxin should be considered early in therapy to help control ventricular response rate. 

Atrial fibrillation is commonly associated with heart failure, and the prevalence of atrial fibrillation is related to the severity of heart failure, with less than 5% affected with very mild heart failure to nearly 50% affected with advanced heart failure [66]. Heart failure and atrial fibrillation are both common cardiovascular disorders and share the same demographic risk factors, including age, history of hypertension, prior myocardial infarction, and valvular heart disease [67, 68]. Further, the incidence of heart failure increases dramatically after the diagnosis of atrial fibrillation [69]. Progression of LV dysfunction can clearly be associated with rapid ventricular rates [70-76]. Conversely, conversion to normal sinus rhythm or control of ventricular response in atrial fibrillation can improve LV function [71-74, 77]. Accordingly, rate control becomes very important in patients with heart failure and dilated cardiomyopathy, and likely even more so when ischemia from rapid rates complicate the patient s course. 

Primary indications for the use of quinidine include (1) abolition of premature complexes that have an atrial, A-V junctional, or ventricular origin (2) restoration of normal sinus rhythm in atrial flutter and atrial fibrillation after controlling the ventricular rate with digitahs (3) maintenance of normal sinus rhythm after electrical conversion of atrial arrhythmias (4) prophylaxis against arrhythmias associated with electrical countershock (5) termination of ventricular tachycardia and (6) suppression of repetitive tachycardia associated with Wolff-Parkinson-White (WPW) syndrome. 

Propranolol alone or in conjunction with digitalis can help control the ventricular rate in patients with atrial flutter or atrial fibrillation. Patients with supraventricular extrasystoles and intermittent paroxysms of atrial fibrillation may benefit from (3-receptor blockade with propranolol. 

Unlabeled Uses Control of hemodynamicallystableventriculartachycardia, control of rapid ventricular rate due to accessory pathway conduction in preexcited atrial arrhythmias, conversion of atrial fibrillation to normal sinus rhythm, in cardiac arrest with persistent ventricular tachycardia or ventricular fibrillation, paroxysmal supraventricular tachycardia, polymorphic ventricular tachycardia or wide complex tachycardia of uncertain origin, prevention of postoperative atrial fibrillation... 

Maintenance dosage for CHF control of ventricular rate in patients with atrial fibrillation treatment and prevention of recurrent paroxysmal atrial tachycardia PO, IV... 

Arrhythmias, including prevention of recurrent paroxysmal supraventricular tachycardia and control of ventricular resting rate in chronic atrial fibrillation or flutter (with di-goxin) PO 240-480 mg/day in 3-4 divided doses. 

Digitalis is the drug of choice in atrial fibrillation for controlling ventricular rate. Its effect is due to the prolongation of the refractory period of the conducting tissue. The dose in so adjusted as to maintain the ventricular rate of 60 to 80 beats per minute at rest and approximately 100 beats per minute during light exercise. 

It is indicated in PSVT, to control ventricular rate in atrial flutter or atrial fibrillation. 

Digitalis is useful in the management of atrial arrhythmias because of its cardioselective parasympathomimetic effects. In atrial flutter and fibrillation, the depressant effect of the drug on atrioventricular conduction helps to control an excessively high ventricular rate. Digitalis has also been used in the control of paroxysmal atrial and atrioventricular nodal tachycardia. At present, calcium channel blockers and adenosine... 

Recent evidence indicates that many patients with atrial fibrillation—a very common arrhythmia in the elderly—do as well with simple control of ventricular rate as with conversion to normal sinus rhythm. Measures (such as anticoagulant drugs) should be taken to reduce the risk of thromboembolism in chronic atrial fibrillation. 

Drugs that block beta-1 receptors on the myocardium are one of the mainstays in arrhythmia treatment. Beta blockers are effective because they decrease the excitatory effects of the sympathetic nervous system and related catecholamines (norepinephrine and epinephrine) on the heart.5,28 This effect typically decreases cardiac automaticity and prolongs the effective refractory period, thus slowing heart rate.5 Beta blockers also slow down conduction through the myocardium, and are especially useful in controlling function of the atrioventricular node.21 Hence, these drugs are most effective in treating atrial tachycardias such as atrial fibrillation.23 Some ventricular arrhythmias may also respond to treatment with beta blockers. 

These agents appear to be similar in efficacy to verapamil in the management of supraventricular arrhythmias, including rate control in atrial fibrillation. An intravenous form of diltiazem is available for the latter indication and causes hypotension or bradyarrhythmias relatively infrequently. Bepridil also has action potential- and QT-prolonging actions that theoretically may make it more useful in some ventricular arrhythmias but also create the risk of torsade de pointes. Bepridil is only rarely used, primarily to control refractory angina. 

Endogenous norepinephrine stimulates cardiac beta receptors. Receptor-linked cAMP-dependent protein kinases phosphorylate calcium channels to increase intracellular calcium. Elevated intracellular calcium increases conduction velocity (phase 0) and decreases the threshold potential in normal SA and AV node cells (see Figure 12.13). Beta blockers slow spontaneous conduction velocity in the SA node by approximately 10-20 percent. In addition, beta blockers can slow conduction velocity while increasing the refractory period of the AV node. These effects control the ventricular rate in atrial fibrillation or flutter and terminate paroxysmal supraventricular tachycardias. They are also safer, although somewhat less effective, than other drugs for suppression of premature ventricular complexes (PVCs). Drugs in this class approved by the FDA for treatment of various arrhythmias include propranolol, acebutolol, and esmolol. Problems with the beta blockers include drowsiness, fatigue, impotence, and depressed ventricular performance. 

Digoxin (see p. 158) shortens the refractory period in atrial and ventricular myocardial cells while prolonging the effective refractory period and diminishing conduction velocity in Purkinje fibers. Digoxin is used to control the ventricular response rate in atrial fibrillation and flutter. At toxic concentrations, digoxin causes ectopic ventricular beats that may result in ventricular tachycardia and fibrillation. [Note This arrhythmia is usually treated with lidocaine or phenytoin.]... 

Digitoxin has an elimination half-life of approximately 7 days and its elimination is relatively unaffected by decreased renal function. For this latter reason, the decision is made to use this drug to control ventricular rate in a 60-year-old man with atrial fibrillation and a creatinine clearance of 25 mL/min. 

Atrial flutter, benefiting by the vagus nerve action of shortening the refractory period of the atrial muscle so that flutter is converted to fibrillation (in which state the ventricular rate is more readily controlled). Electrical cardioversion is preferred. 

C Diltiazem. Quinidine can be used to maintain normal sinus rhythm (NSR) after cardioversion of atrial fibrillation. Metoprolol is commonly used to control ventricular rate before conversion to NSR. However, this patient has two contraindications (COPD and diabetes) for beta-blocker use. Unlike diltiazem, amlodipine and nimodipine do not block AV nodal conduction therefore, they would be ineffective at rate control. 

Digitalis glycosides are positive inotropic agents used in the management of patients with congestive heart failure. They control ventricular rate in supraventricular arrhythmias including atrial fibrillation and atrial flutter. 

Use PO Treatment of angina due to Half-life Onset Peaks Duration coronary artery spasm (Prinzmetal s 3-8 hours PO 30-60 6-12 h 24 hours variant angina), chronic stable minutes angina (effort-associated angina). IV Immediate Extended release Treatment of essential hypertension and angina. Parenteral Temporary control of rapid ventricular rate in atrial fibrillation/flutter. Rapid conversion of PSVT to normal sinus rhythm. 

Arterial pulses are an accurate measure of the ventricular rate in healthy persons with good ventricular function. In patients with a rapid ventricular rate—because of supraventricular tachyarrhythmias such as atrial flutter or fibrillation or rapid ventricular rates (e.g., ventricular tachycardia or premature ventricular beats)—extremity pulses (e.g., radial pulse) may be considerably slower than the true ventricular rate. A more accurate ventricular rate is determined by listening to the ventricles with the stethoscope (usually at the apex) or counting from an ECG. In patients with atrial fibrillation and a fast ventricular rate, a pulse deficit (measure of the difference in true ventricular rate and peripheral pulse rate) may exist. This may be as much as 10 to 20 beats per minute. Thus the location of the pulse (radial or apical) should be recorded. The pulse deficit will be reduced as the ventricular rate is controlled with drug therapy or normal sinus rhythm is restored. 

---